ArticleEukaryotic cell2011
The yeast-phase virulence requirement for α-glucan synthase differs among Histoplasma capsulatum chemotypes.
Article in Eukaryotic cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 72 citations in OpenAlex.
- Genotypic diversity, virulence, and molecular genetic tools inMicrobiology and molecular biology reviews : MMBR · 2024Review
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- Phenotypic characterization of cryptic species in the fungal pathogenbioRxiv : the preprint server for biology · 2024Article
- Targeted gene deletions in the dimorphic fungal pathogenmSphere · 2023Article
- Fungal resilience and host-pathogen interactions: Future perspectives and opportunities.Parasite immunology · 2023Review
- Key thermally dimorphic fungal pathogens: shaping host immunity.Open biology · 2022Review
- An Indian lineage of Histoplasma with strong signatures of differentiation and selection.Fungal genetics and biology : FG & B · 2022Article
- Fungal α-1,3-Glucan as a New Pathogen-Associated Molecular Pattern in the Insect Model HostMolecules (Basel, Switzerland) · 2021Article
- Fungal immunity and pathogenesis in mammals versus the invertebrate model organism Galleria mellonella.Pathogens and disease · 2021Review
- Comparative Proteomic Analysis ofFrontiers in microbiology · 2021Article
- BiodiversemSphere · 2020Article
- Heat Shock Protein 60, Insights to Its Importance inFrontiers in cellular and infection microbiology · 2020Article
- Sensing the heat and the host: Virulence determinants ofVirulence · 2019Review
- How Environmental Fungi Cause a Range of Clinical Outcomes in Susceptible Hosts.Journal of molecular biology · 2019Review
- Flying under the radar: Histoplasma capsulatum avoidance of innate immune recognition.Seminars in cell & developmental biology · 2019Review
- Metabolic Peculiarities ofFrontiers in microbiology · 2019Article
- Histoplasma Capsulatum: Mechanisms for Pathogenesis.Current topics in microbiology and immunology · 2019Review
- Characterization of the APSES-family transcriptional regulators of Histoplasma capsulatum.FEMS yeast research · 2018Article
- O-Mannosylation of Proteins EnablesmBio · 2018Article
- Differentiation of the fungus Histoplasma capsulatum into a pathogen of phagocytes.Current opinion in microbiology · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Histoplasma capsulatum strains can be classified into two chemotypes based on cell wall composition. The cell wall of chemotype II yeast contains a layer of α-(1,3)-glucan that masks immunostimulatory β-(1,3)-glucans from detection by the Dectin-1 receptor on host phagocytes. This α-(1,3)-glucan cell wall component is essential for chemotype II Histoplasma virulence. In contrast, chemotype I yeast cells lack α-(1,3)-glucan in vitro, yet they remain fully virulent in vivo. Analysis of the chemotype I α-glucan synthase (AGS1) locus revealed a 2.7-kb insertion in the promoter region that diminishes AGS1 expression. Nonetheless, AGS1 mRNA can be detected during respiratory infection with chemotype I yeast, suggesting that α-(1,3)-glucan could be produced during in vivo growth despite its absence in vitro. To directly test whether AGS1 contributes to chemotype I strain virulence, we prevented AGS1 function by RNA interference and by insertional mutation. Loss of AGS1 function in chemotype I does not impair the cytotoxicity of ags1(-) mutant yeast to cultured macrophages, nor does it affect the intracellular growth of yeast. In a murine model of histoplasmosis, the ags1(-) chemotype I mutant strains show no defect in lung infection or in extrapulmonary dissemination. Together, these studies demonstrate that AGS1 expression is dispensable for chemotype I yeast virulence, in contrast to the case for chemotype II yeast. Despite the absence of cell wall α-(1,3)-glucan, chemotype I yeast can avoid detection by Dectin-1 in a growth stage-dependent manner. This suggests the production of a unique Histoplasma chemotype I factor that, at least partially, circumvents the α-(1,3)-glucan requirement for yeast virulence.
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